Journal
VIRULENCE
Volume 4, Issue 6, Pages 467-472Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/viru.25641
Keywords
Acinetobacter baumannii; alcohol; cytokines; macrophages; phagocytosis
Categories
Funding
- NIH-NIAID [5K22A108781702]
- Long Island University-Post Faculty Research Committee Awards
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Acinetobacter baumannii (Ab) is a common cause of community-acquired pneumonia (CAP) in chronic alcoholics in tropical and sub-tropical climates and associated with a >50% mortality rate. We demonstrated that exposure of J774.16 macrophage-like cells to physiological alcohol (EtOH) concentrations decreased phagocytosis and killing of Ab. EtOH-mediated macrophage phagocytosis dysfunction may be associated with reduced expression of GTPase-RhoA, a key regulator of the actin polymerization signaling cascade. EtOH inhibited nitric oxide (NO) generation via inducible NO-synthase inactivation, which enhanced Ab survival within macrophages. Additionally, EtOH alters cytokine production resulting in a dysregulated immune response. This study is a proof of principle which establishes that EtOH might exacerbate Ab infection and be an important factor enhancing CAP in individuals at risk.
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